Mutations of PTPN23 in developmental and epileptic encephalopathy.
Nadine SowadaMais Omar HashemRüstem YilmazMuddathir HamadNaseebullah KakarHolger ThieleStefan T AroldHarald BodeFowzan S AlkurayaGuntram BorckPublished in: Human genetics (2017)
Developmental and epileptic encephalopathies (DEE) are a heterogeneous group of neurodevelopmental disorders with poor prognosis. Recent discoveries have greatly expanded the repertoire of genes that are mutated in epileptic encephalopathies and DEE, often in a de novo fashion, but in many patients, the disease remains molecularly uncharacterized. Here, we describe a new form of DEE in patients with likely deleterious biallelic variants in PTPN23. The phenotype is characterized by early onset drug-resistant epilepsy, severe and global developmental delay, microcephaly, and sometimes premature death. PTPN23 encodes a tyrosine phosphatase with strong brain expression, and its knockout in mouse is embryonically lethal. Structural modeling supports a deleterious effect of the identified alleles. Our data suggest that PTPN23 mutations cause a rare severe form of autosomal-recessive DEE in humans, a finding that requires confirmation.
Keyphrases
- early onset
- poor prognosis
- drug resistant
- late onset
- long non coding rna
- intellectual disability
- multidrug resistant
- end stage renal disease
- acinetobacter baumannii
- ejection fraction
- newly diagnosed
- chronic kidney disease
- peritoneal dialysis
- copy number
- dna methylation
- genome wide
- resting state
- prognostic factors
- white matter
- patient reported outcomes
- binding protein
- multiple sclerosis
- functional connectivity
- cystic fibrosis
- duchenne muscular dystrophy
- cerebral ischemia